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应用表型药物发现策略来确定抑制肺上皮细胞中TSLP产生的生物学和化学起始点。

Application of a phenotypic drug discovery strategy to identify biological and chemical starting points for inhibition of TSLP production in lung epithelial cells.

作者信息

Orellana Adelina, García-González Vicente, López Rosa, Pascual-Guiral Sonia, Lozoya Estrella, Díaz Julia, Casals Daniel, Barrena Antolín, Paris Stephane, Andrés Miriam, Segarra Victor, Vilella Dolors, Malhotra Rajneesh, Eastwood Paul, Planagumà Anna, Miralpeix Montserrat, Nueda Arsenio

机构信息

Almirall R&D Center, Almirall S.A., Sant Feliu de Llobregat, Barcelona, Spain.

出版信息

PLoS One. 2018 Jan 10;13(1):e0189247. doi: 10.1371/journal.pone.0189247. eCollection 2018.

Abstract

Thymic stromal lymphopoietin (TSLP) is a cytokine released by human lung epithelium in response to external insult. Considered as a master switch in T helper 2 lymphocyte (Th2) mediated responses, TSLP is believed to play a key role in allergic diseases including asthma. The aim of this study was to use a phenotypic approach to identify new biological and chemical starting points for inhibition of TSLP production in human bronchial epithelial cells (NHBE), with the objective of reducing Th2-mediated airway inflammation. To this end, a phenotypic screen was performed using poly I:C / IL-4 stimulated NHBE cells interrogated with a 44,974 compound library. As a result, 85 hits which downregulated TSLP protein and mRNA levels were identified and a representative subset of 7 hits was selected for further characterization. These molecules inhibited the activity of several members of the MAPK, PI3K and tyrosine kinase families and some of them have been reported as modulators of cellular phenotypic endpoints like cell-cell contacts, microtubule polymerization and caspase activation. Characterization of the biological profile of the hits suggested that mTOR could be a key activity involved in the regulation of TSLP production in NHBE cells. Among other targeted kinases, inhibition of p38 MAPK and JAK kinases showed different degrees of correlation with TSLP downregulation, while Syk kinase did not seem to be related. Overall, inhibition of TSLP production by the selected hits, rather than resulting from inhibition of single isolated targets, appeared to be due to a combination of activities with different levels of relevance. Finally, a hit expansion exercise yielded additional active compounds that could be amenable to further optimization, providing an opportunity to dissociate TSLP inhibition from other non-desired activities. This study illustrates the potential of phenotypic drug discovery to complement target based approaches by providing new chemistry and biology leads.

摘要

胸腺基质淋巴细胞生成素(TSLP)是人类肺上皮细胞在受到外部刺激时释放的一种细胞因子。TSLP被认为是辅助性T细胞2(Th2)介导的免疫反应中的一个主开关,据信在包括哮喘在内的过敏性疾病中起关键作用。本研究的目的是采用表型分析方法,确定抑制人支气管上皮细胞(NHBE)中TSLP产生的新生物学和化学起始点,以减少Th2介导的气道炎症。为此,使用聚肌胞苷酸/白细胞介素-4刺激的NHBE细胞,对一个包含44974种化合物的文库进行表型筛选。结果,鉴定出85种能下调TSLP蛋白和mRNA水平的活性化合物,并选择了7种具有代表性的活性化合物进行进一步表征。这些分子抑制了丝裂原活化蛋白激酶(MAPK)、磷脂酰肌醇-3激酶(PI3K)和酪氨酸激酶家族中几个成员的活性,其中一些已被报道为细胞表型终点(如细胞间接触、微管聚合和半胱天冬酶激活)的调节剂。对这些活性化合物生物学特性的表征表明,雷帕霉素靶蛋白(mTOR)可能是参与调节NHBE细胞中TSLP产生的关键活性物质。在其他靶向激酶中,抑制p38 MAPK和Janus激酶(JAK)与TSLP下调表现出不同程度的相关性,而脾酪氨酸激酶(Syk)似乎与之无关。总体而言,所选活性化合物对TSLP产生的抑制作用,似乎并非源于对单个孤立靶点的抑制,而是不同相关水平活性的综合作用。最后,通过活性化合物扩展实验得到了其他可进一步优化的活性化合物,这为将TSLP抑制与其他非期望活性分离提供了机会。本研究说明了表型药物发现通过提供新的化学和生物学线索来补充基于靶点方法的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8611/5761851/8d80153f0ae2/pone.0189247.g001.jpg

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